Evidence map›Paper›PMID 18381943›Full record

Trial reportClinical cancer research : an official journal of the American Association for Cancer Research2008

Single-nucleotide polymorphisms of DNA damage response genes are associated with overall survival in patients with pancreatic cancer.

Taro Okazaki, Li Jiao, Ping Chang, Douglas B Evans, James L Abbruzzese, Donghui Li

Abstract readClinical Trial, Phase II
In one paragraph

Trial report in Clinical cancer research : an official journal of the American Association for Cancer Research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 54 citations in OpenAlex.

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  17. A replication study and genome-wide scan of single-nucleotide polymorphisms associated with pancreatic cancer risk and overall survival.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
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  18. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Taro OkazakiDepartment of Gastrointestinal Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
Li Jiao
Ping Chang
Douglas B Evans
James L Abbruzzese
Donghui Li
The University of Texas MD Anderson Cancer Center · USDivision of Cancer Epidemiology and Genetics

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Jared Kyle Burks · 1985 to 2026
$290.8M
SPORE in Pancreatic CancerP20CA101936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABBRUZZESE, JAMES L. · 2003 to 2009
$5.4M
Molecular Epidemiology of Pancreatic CancerR01CA098380 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, DONGHUI · 2004 to 2008
$2.6M
NCI NIH HHS CA16672NCI NIH HHS P20 CA101936NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA098380
6 · The paper itself

Abstract

purposeThe goals of this study were to determine if single-nucleotide polymorphisms in DNA damage repair genes and cell cycle regulating genes affect clinical response to combined gemcitabine radiation therapy and the overall survival (OS) of patients with pancreatic cancer. EXPERIMENTAL

designWe evaluated six single-nucleotide polymorphisms of the ATM, ATM and Rad3-related (ATR), CHEK1, and CHEK2 genes in 119 patients with potentially resectable pancreatic cancer who were enrolled in clinical trials at The University of Texas M. D. Anderson Cancer Center from February 1999 to January 2006, with follow-up until February 2007. Patients received neoadjuvant concurrent gemcitabine and radiation therapy with or without gemcitabine-cisplatin induction therapy. Genotypes were determined and tested for associations with OS by Kaplan-Meier estimation, the log-rank test, and Cox regression analysis. P values of <or=0.05 were considered significant.

resultsThe ATM G60A and CHEK1 G35A genotypes were significant (P<0.05), and the ATR C340T genotype borderline significantly (P=0.079) associated with OS. The hazard ratio of CHEK1 35AA was 2.01 (95% confidence interval, 1.20-3.37; P=0.007) compared with CHEK1 35GG/GA with adjustments for race, sex, diabetes status, CA19-9 level, and success of tumor resection. A significant combined genotype effect was observed between ATM 60GA/GG, ATR 340CT/CC, and CHEK1 35AA with median OS times of 31.0, 16.2, and 10.5 months for patients carrying <or=1, 2, and 3 deleterious alleles, respectively (P=0.004).

conclusionsThese observations suggest that polymorphic variations of DNA damage response genes affect clinical response to gemcitabine radiation therapy and OS of patients with resectable pancreatic cancer.

Indexed as

Polymorphism, Single NucleotideAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorCarcinoma, Pancreatic DuctalCisplatinDeoxycytidineDNA DamageGemcitabineGenotypeHumansKaplan-Meier EstimatePancreatic NeoplasmsRadiotherapyBiomarkers, TumorCisplatinDeoxycytidineGemcitabine

Identifiers

PMID18381943
PMCPMC2423806
OpenAlexW2117271731

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.